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1 ilized as an adjuvant therapeutic to enhance radiation sensitivity.
2 mitotic catastrophe and a modest increase in radiation sensitivity.
3  within the tumours without increasing their radiation sensitivity.
4 n increases in C16 ceramide accumulation and radiation sensitivity.
5 ely target such cells for potential enhanced radiation sensitivity.
6  cell cycle checkpoint defects, and ionizing radiation sensitivity.
7  methyl methanesulfonate, but only slight UV radiation sensitivity.
8  determine if PI 3-kinase activity regulates radiation sensitivity.
9 t lead to perceptible alterations in drug or radiation sensitivity.
10 therapy, to identify parameters that predict radiation sensitivity.
11 e and adaptive immunity as key correlates of radiation sensitivity.
12  the miR-99 family of miRNAs correlates with radiation sensitivity.
13 NAs with the doubling-time of cells or their radiation sensitivity.
14 because refractory disease typically retains radiation sensitivity.
15 ination of H2AX profoundly enhances ionizing radiation sensitivity.
16 esistant to many anticancer agents, enhances radiation sensitivity.
17 features to identify parameters that predict radiation sensitivity.
18 cing had a minimal effect on NL20 growth and radiation sensitivity.
19  predisposition, chromosomal instability and radiation sensitivity.
20 omosome instability, DNA repair defects, and radiation sensitivity.
21 n therapy, we studied MSI1 in the context of radiation sensitivity.
22 identification of novel molecular markers of radiation sensitivity.
23 IP76 via a liposomal delivery system rescued radiation sensitivity.
24  which expression values are correlated with radiation sensitivity.
25 on of DNA-PKcs at these sites show increased radiation sensitivity.
26 n+/-mice were equivalent to p53 null mice in radiation sensitivity.
27  independent pathway leading to induction of radiation sensitivity.
28 and SKMG-3 cells, rapamycin had no impact on radiation sensitivity.
29 hairpin ends and increased cellular ionizing radiation sensitivity.
30 etion of the ubiquitin-like domain causes UV radiation sensitivity.
31 terogeneous mix of cell types with differing radiation sensitivities.
32                        Differential ionizing radiation sensitivities among the hypomorphic mre11 alle
33 nt cells demonstrate an increase in ionizing radiation sensitivity and a decrease in DNA DSB repair a
34 rmore, depletion of ubc-9 and tac-1 leads to radiation sensitivity and a high incidence of males, res
35 strand break detection resulting in cellular radiation sensitivity and a predisposition to cancer.
36 dant, hydroxyethyldisulfide, caused enhanced radiation sensitivity and an inability to repair DNA dou
37 2 expression have phenotypic consequences on radiation sensitivity and cancer predisposition.
38  into why BRCA2 C-terminal deletions lead to radiation sensitivity and cancer predisposition.
39 pect to other checkpoint functions, ionizing radiation sensitivity and chromosome stability.
40  exhibiting these interactions had increased radiation sensitivity and decreased ability to repair do
41 normalities such as chromosomal instability, radiation sensitivity and defects in cell-cycle checkpoi
42 zygous for null alleles of atm reproduce the radiation sensitivity and high-tumor incidence of the hu
43          Mutation of Thr2609 to Ala leads to radiation sensitivity and impaired DSB rejoining.
44 ential clinical significance with respect to radiation sensitivity and local control will be highligh
45 AD50, and XRS2 are characterized by ionizing radiation sensitivity and mitotic interhomologue hyperre
46 s about the generality of the role of ATM in radiation sensitivity and the potential use of ATM inhib
47 patients, including chromosomal instability, radiation sensitivity, and aberrant cell-cycle-checkpoin
48 actate production, PKM1 and PKM2 expression, radiation sensitivity, and cell cycle duration of GSCs a
49 nduced cell-cycle checkpoints, apoptosis and radiation sensitivity, and cellular proliferation.
50 tal arrest in Brca2-deficient embryos, their radiation sensitivity, and the association of Brca2 with
51 and composition when evaluating biomaterials radiation sensitivity, and to the development of strateg
52  role of DNA-PKcs in lymphocyte development, radiation sensitivity, and tumorigenesis, we disrupted t
53 netic loss of atm and p21 on growth control, radiation sensitivity, and tumorigenesis.
54                    In our approach, we treat radiation sensitivity as a continuous variable, signific
55                        Consistent with this, radiation sensitivity, as measured by clonogenic assay o
56  transport capacity and stepwise increase in radiation sensitivity associated with heterozygous or ho
57        HPV+ HNCs exhibited greater intrinsic radiation sensitivity (average SF2 HPV-: 0.59 vs. HPV+:
58                            We establish that radiation sensitivity can be predicted based on gene exp
59 phenotypes, including cancer predisposition, radiation sensitivity, cell-cycle checkpoint defects, im
60 e syndrome (NBS) is characterized by extreme radiation sensitivity, chromosomal instability and cance
61 karyotic elongation factor-2 (eEF-2) kinase, radiation sensitivity complementing kinase-2 (RCK-2), an
62 er a patient-specific molecular signature of radiation sensitivity could be used to identify the opti
63 SS-depleted cells display increased ionizing radiation sensitivity, defective G2/M checkpoint, and im
64 Nbs1 and Mre11 are responsible for the human radiation sensitivity disorders Nijmegen breakage syndro
65 gue recombination, chromosome loss, ionizing radiation sensitivity, double-strand break repair, and p
66 ited syndrome ataxia telangiectasia, exhibit radiation sensitivity, fertility defects, and are T-cell
67 s a recessive human disease characterized by radiation sensitivity, genetic instability, immunodefici
68            Whether apoptosis is required for radiation sensitivity has been controversial.
69 ne pathways involved in tumor initiation and radiation sensitivity have been identified.
70  and molecularly targeted therapy to enhance radiation sensitivity have contributed equally to the im
71 ses to DSBs, such as cell cycle checkpoints, radiation sensitivity, immune dysfunction, infertility a
72 angiectasia characteristics such as ionizing radiation sensitivity, immunodeficiency, and infertility
73 PD52, and DEPDC1B each significantly altered radiation sensitivity in at least two cancer cell lines.
74 MLH1 produced a further increase in ionizing radiation sensitivity in both SW620 and HCT116 1-2 cells
75  inhibition of Akt phosphorylation increases radiation sensitivity in clonogenic assays, suggesting t
76 hd analogue in DNA, there was an increase in radiation sensitivity in HCT116 cells but not in HCT116/
77 e, and a supporting mechanism, for increased radiation sensitivity in HPV+ HNC relative to HPV- HNC.
78       ATR can functionally complement esr1-1 radiation sensitivity in S. cerevisiae.
79 mic lymphomagenesis and an increase in acute radiation sensitivity in vivo (the latter principally be
80                             IC87361 enhanced radiation sensitivity in wild-type C57BL6 endothelial ce
81 onal, because mutations in this motif confer radiation sensitivity in yeast and disrupt binding at th
82            We used the gene-expression-based radiation-sensitivity index and the linear quadratic mod
83 n cell-cycle checkpoint mutants and that the radiation sensitivity is a consequence of this defect.
84       Another factor that critically affects radiation sensitivity is cell-cycle regulation.
85                                          The radiation sensitivity is dependent on the size of the ma
86 the RAD3 epistasis group by quantitating the radiation sensitivities of dun1, rad52, rad1, rad9, rad1
87 haracteristic can be utilized to compare the radiation sensitivities of these proteins in the two sta
88                                 The ionizing radiation sensitivity of a mutant defective for extensiv
89           We systematically investigated the radiation sensitivity of all available validated HPV+ HN
90         Although little effect of p53 on the radiation sensitivity of asynchronously growing cultures
91 nuclease, was found to increase the ionizing radiation sensitivity of both mre11Delta and mre11-H125N
92 ate, to examine the cell cycle dependence of radiation sensitivity of Brca2(Tr/Tr)/p53(-/-) compared
93 radation after IR may be responsible for the radiation sensitivity of CD34+ cells compared with tumor
94  expression of p16INK4a dramatically affects radiation sensitivity of HNSCC cells.
95 s study, we investigated the role of Prx1 in radiation sensitivity of human lung cancer cells, with s
96 have examined this question by measuring the radiation sensitivity of human tumor cell lines with onc
97 ated by virtue of its ability to correct the radiation sensitivity of irs1SF cells.
98                                   Studies of radiation sensitivity of long-term engrafting cells have
99                                     Enhanced radiation sensitivity of MIA PaCa-2/RII cells was associ
100 promote chromosomal instability and increase radiation sensitivity of mouse fibroblasts.
101 Ku70 (yKu70) deficiency reduces the ionizing radiation sensitivity of mre11Delta mutants.
102 to interact with Mre11 and to complement the radiation sensitivity of NBS cells.
103 n vitro, whereas NS-123 did not increase the radiation sensitivity of normal human astrocytes or deve
104 ild-type p16INK4a (Ad/p16) expression on the radiation sensitivity of NSCLC cell lines, all of which
105                    The results show that the radiation sensitivity of proteins depends on the mass of
106 ed by a complete suppression of the ionizing radiation sensitivity of rad55 or rad57 mutants by conco
107 0 fusion protein is also active in restoring radiation sensitivity of rec2 but is hyperactive to an e
108 ive of this study was to compare the in situ radiation sensitivity of recombinant human granulocyte c
109 can complement the slow growth phenotype and radiation sensitivity of S.pombe rad31.
110 aluating molecular markers as they relate to radiation sensitivity of solid tumors.
111                          Results confirm the radiation sensitivity of the breast in girls age 10 to 2
112  of a dominant negative MEK1 does not affect radiation sensitivity of the cell, the G2/M checkpoint o
113  highest activity in suppression of ionizing radiation sensitivity of the rad57 mutant, and Val 328 a
114 raction could be targeted for enhancing drug/radiation sensitivity of tumor cells.
115 ic response and constituting a mechanism for radiation sensitivity or resistance.
116 c response, thus constituting a mechanism of radiation sensitivity or resistance.
117           There was no evidence of increased radiation sensitivity or sequelae in breast tissue heter
118 zation, but reduced NPM level does not alter radiation sensitivity per se.
119 treatment of HT-29 cells with U0126 enhanced radiation sensitivity possibly due to the accumulation o
120              The development of a successful radiation sensitivity predictive assay has been a major
121 expressing an undegradable BLM mutant showed radiation sensitivity, probably by triggering end resect
122                      The estimated values of radiation sensitivity (represented as SF2, the survival
123 owing RNF8 depletion, and mitigated ionizing radiation sensitivity resulting from RNF8 deficiency.
124                                              Radiation sensitivity studies also indicate that hyperth
125 s, inhibition of autophagy promotes enhanced radiation sensitivity through a mechanism that requires
126      Importantly, LRF loss restores ionizing radiation sensitivity to p53 null cells, making LRF an a
127                                              Radiation sensitivity was demonstrated in trophectoderm-
128  tonsillar epithelial (HTE) cells, increased radiation sensitivity was seen in cell expressing HPV-16
129     The influence of autophagy inhibition on radiation sensitivity was studied in human breast, head
130 influence of the chromosome 17-linked QTL on radiation sensitivity, we conducted studies on congenic
131 on tests showed that Nrf2 deletion increased radiation sensitivity, whereas Nrf2-inducing drugs did n

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